Cpap

[Chrissy1]

Hello
I live in a rural area and we are just getting CPAP on one of the services I work with and the other has had it for a while. I used it for the first time a couple weeks ago and it helped so much more then either of us in the back though it could. I understand how it works but I am still not sure about using it. I just want a few other opinions. In class all we got was this is a CPAP. This is how it works. When you need to set it up you can figure it out. Your pt must be conscious to use it.
What do you guys think of it? What have you used it for?

 

[NomadicMedic]

Hello
I live in a rural area and we are just getting CPAP on one of the services I work with and the other has had it for a while. I used it for the first time a couple weeks ago and it helped so much more then either of us in the back though it could. I understand how it works but I am still not sure about using it. I just want a few other opinions. In class all we got was this is a CPAP. This is how it works. When you need to set it up you can figure it out. Your pt must be conscious to use it.
What do you guys think of it? What have you used it for?

What do you want "opinions" for? I'm sure you have protocols that specify when it is to be used, right?

It's used (in most cases) for patients with Pulmonary Edema, secondary to CHF. In some areas it is also used, in conjunction with nebulized Beta agonists, for COPD and asthma.

If you don’t understand its use or function and if you haven’t been fully trained on it, it’s not a tool you should be using. Another example of EMS education putting skills ahead of true education.

 

[fast65]

I think it's a great tool, and one that when used appropriately, helps to stave on intubation in the APE patient. Every time I've used it, the patient seemed to turn around with the drop of a hat, unfortunately, we aren't allowed to use it for asthma...yet.

That being said, it's a treatment (like any other treatment) that you need to be knowledgable about, prior to using it on a patient.

 

[Outbac1]

Great tool! I love having it as an option. I've used it several times and only once did it not have a positive effect. The pt got tubed. The others all had good outcomes. Two of which needed nothing more after arrival at the ER.

We use I believe a Miller device which has a guage on it. It requires 15 -25lpm of O2 to operate. A couple of nurses don't like it on the COPDers as we "give too much oxygen" and want to turn it down to 2lpm. With that low of flow there is no pressure. The RTs would rather fix the Co2 with their BiPap than have the pt tubed and on the vent.

Our indications are generous in that the pt needs to be
>16yo
co-operative / patent airway
severe dyspnea

and two of the following

respiratory rate>24
spo2<90%
skin signs
adventitous sounds

Here all levels of paramedic can use it.

 

[BLS Systems Limited]

You really have to have a good grasp of the A&P to fully comprehend the function and benefits of CPAP. It has been used in hospitals for a couple of decades for CHF/APE but they had unlimited access to power and oxygen reserves. Only in the last 10 years have reliable, easy to use units been available for out of hospital application where it has been shown to decrease intubation by 50% or more. The success largely depends on far along the patient is. As mentioned above, not every service uses it for all forms of SOB.

One of the biggest confusing factors is the application of CPAP for sleep apnea versus CHF/APE...different devices to solve different problems. There are more and more presentations on how CPAP for CHF/APE function. A quick Google search should reveal what you need to build on what you already know. If not, feel free to contact me off thread and I may be able to send you what I have.

 

[18G]

Chrissy...

CPAP exerts a positive pressure in the chest (as the name implies but worth restating) and provides a beneficial hemodynamic effect by reducing preload and afterload.

The positive pressure exerted in the chest impinges on the vena cava causing blood return to the heart to be reduced. With reduced blood return comes reduced blood volume that the heart has to worry about pumping out. In other words reduced myocardial oxygen demand and relief for the already strained heart.

In CHF management, the immediate goal is to reduce pressure in the pulmonary vasculature to reduce the pressure gradient so that fluid can start to retreat back across the A-C membrane which decreases diffusion distance and improves gas exchange. This is why the priority is aggressive nitro dosing and CPAP and NOT lasix.

There is also a possibility of a negative hemodynamic effect. If your patient is already running a low B/P, the PEEP from CPAP may cause hypotension. In your CHF patient chances are the hormonal and sympathetic response is going to cause your patient's B/P to be elevated but not always so not a great concern but you definitely need to be aware of the hemodynamic effects involved with CPAP.

The mechanism in which CPAP works in Asthma and COPD is less understood and is debated. But it has been shown to reduce the work of breathing and is often effective when patients are refractory to traditional treatments.

Also, if you have it available... use a nasal cannula type EtCO2 filter line under the CPAP mask. It will not effect your mask seal.

Normally, your PEEP pressure is 5-10cmH20. Start at 5 and titrate up to 10. I usually do 5-7-10. As long as your at 10 or below your risks of adverse events are minimal. If your patient is not improving at 10cmH20 and deteriorating your patient is now a candidate for intubation more than likely.

CPAP prevents alveolar collapse by maintaining a constant pressure within them. A partially open airway is much easier to inflate than a closed one. Think of a balloon. When is it easier to inflate?? It's when you already have some air in it. Same concept. Also, with pulmonary edema the alveoli are prone to collapse. Surfactant washout can occur especially with near-drownings. Without surfactant our airways collapse (atelectasis). So CPAP helps mitigate this. This is where the decreased work of breathing comes into play. CPAP also recruits collapsed alveoli and makes them take part in gas exchange.

CPAP also causes increased surface area for gas exchange to occur. CPAP also usually makes bronchodilators more effective when administered inline with the CPAP.

If your not getting good PEEP make sure you have a good mask seal. If not, you will not achieve proper PEEP to be effective.

And very IMPORTANT. ACCLIMATE your patient to the CPAP. Don't just slap it on. Hold it on and coach the patient before securing. If need be, give a low dose benzo to reduce their anxiety. This step is VERY important.

Always remember that your patient has to be able to maintain their own airway. If the patient is or is becoming somnolent or head bobbing... its time to think intubation and bagging these patients.

Use your assessment and tools to gauge patient improvement. You should see SpO2 increase, EtCO2 decrease (could be decreasing cardiac output too in CHF), decreased work of breathing, reduced resp rate, and the patient will tell you if they are feeling better.

Don't be afraid to use CPAP. If unsure, use it. As a new medic I was intimidated by CPAP and quickly learned not to be scared of it. It is pretty harmless if a few basic principles are understood mainly related to the hemodynamic effects.

It sucks your service didn't feel the need to give proper education and training on the new skill of CPAP. Make Google your best friend and if you have any specific questions ask em here. CPAP is a life saver literally and prevents need for intubation. Once some of these patients go on the vent, they don't come off. It really turns em around.

I am exhausted and this all came out on auto-pilot so hopefully it makes sense to ya

 

[socalmedic]

I have to say bravo to what is said above. most books wont give you such concise information.

however I would say that Lasix is just as important as NTG in managing CHF/PE. Lasix's pulmonary vasodilation has effect in 3-5 min and duration for approx 1-2 hours, its use as a diuretic in emergency medicine is more of a side effect than intended action. think of it as similar to Pepsid in an allergic reaction, slower onset but works after the Benadryl stops.

 

[MSDeltaFlt]

Also very mindful of your tank pressure. Different makes and models will use different FiO2's utilizing different flow rates. The more flow that is used the sooner your tank will be depleted. Especially if you have an out of town transfer and they'r on CPAP. If your tank's not full, you might not make it.

 

[Christopher]

I'll add that as long as your patient is breathing adequately, they don't necessarily have to be GCS 15 to use CPAP.

If they're obtunded and wheezy/rhalesy, either CPAP with a jaw thrust or CPAP+Nebs+jaw thrust can go a long way.

Because believe you me, we're all worse with a bag valve mask than spontaneous breathing and CPAP...

 

[Christopher]

however I would say that Lasix is just as important as NTG in managing CHF/PE. Lasix's pulmonary vasodilation has effect in 3-5 min and duration for approx 1-2 hours, its use as a diuretic in emergency medicine is more of a side effect than intended action. think of it as similar to Pepsid in an allergic reaction, slower onset but works after the Benadryl stops.

I'm not so sure the literature agrees. A number of studies have shown that CHF/PulmEdema patients were euvolemic or even hypovolemic and they needed MORE fluid to improve hemodynamics.

Prehospital diuretics are not an effective means of treatment (nor one supported by any research). Papers going back to 1987 have even shown harm with traditional morphine and lasix treatments!

You should instead be switching to IV NTG or an ACE inhibitor such as enalapril.

 

[socalmedic]

I'm not so sure the literature agrees. A number of studies have shown that CHF/PulmEdema patients were euvolemic or even hypovolemic and they needed MORE fluid to improve hemodynamics.

Prehospital diuretics are not an effective means of treatment (nor one supported by any research). Papers going back to 1987 have even shown harm with traditional morphine and lasix treatments!

You should instead be switching to IV NTG or an ACE inhibitor such as enalapril.

which is why I said dieresis is more of a side effect with the vasodilatory effects being what we want. fluid maintenance, and ins/outs are easily measured and corrected for in the ER.

 

[18G]

Lasix is not really recommended routinely anymore especially pre-hospital just as Christopher has mentioned. Some habits die hard which is why it is still commonly used. CPAP and pressure reduction with nitro is what turns these patients around. And not a single nitro every 5mins with a pressure of 185/98.

One NTG protocol for CHF/CPAP is SBP>180 = 3 NTG, 140-180 = 2 NTG and <140 = 1 NTG q5mins.

I like the idea of an ACE inhibitor to reduce afterload. Maryland took this out I believe in their last protocol update. Not sure why. We still have it in PA although some ED docs and nurses are clueless as to why we ask for orders to give captopril in the field for CHF.

 

[blindsideflank]

Not trying to sound like too much of a cookbook here but it's funny that you don't give cpap in a hypotensive pt. Kind of c before a and b. That said if you are hypotensive because the primary problem is pulmonary edema then you have progressed so far that it's intubation and peep time.

Peep and cpap can really be stressful when it's a less defined issue. The rosc with pulmonary edema and a bp of 130... Peep worries me in is pt but I still give it. I'm not sure if it's right. (is per protocol but what does that mean) what if there is definite stemi, are you increasing mv02 or is the hypoxia worse? You don't necessarily even want high o2 in this guy but definitely want to lower mvo2

Those hypotensive chf pt that could use cpap... Anyone get to use dobutamine etc in chf pts?

I've seen gcs 11 on cpap come back to a lethargic 15, but I have never used it on such a pt.

 

[usalsfyre]

Not trying to sound like too much of a cookbook here but it's funny that you don't give cpap in a hypotensive pt. Kind of c before a and b. That said if you are hypotensive because the primary problem is pulmonary edema then you have progressed so far that it's intubation and peep time.

The problem is pulmonary edema is generally a SYMPTOM of an underlying pathology rather than the primary etiology (unless it's something like HAPE). Any PPV is going to hurt you in cardiogenic shock.

Peep and cpap can really be stressful when it's a less defined issue. The rosc with pulmonary edema and a bp of 130... Peep worries me in is pt but I still give it. I'm not sure if it's right. (is per protocol but what does that mean) what if there is definite stemi, are you increasing mv02 or is the hypoxia worse? You don't necessarily even want high o2 in this guy but definitely want to lower mvo2

APE and a pressure of 130 seems like a LV that is very sick and a vascular system thats having issues on top of it. I'm not sure I follow you about CPAP being stressful and increasing MvO2. Your generally looking at CPAP decreasing workload as your shedding preload.

Those hypotensive chf pt that could use cpap... Anyone get to use dobutamine etc in chf pts?

Unless you're sure your looking at straight systolic failure with no valvular or aortic disease AND are trying to reduce afterload (very tough to determine in the field) leave the inotropes alone, bad things can happen quick.

I've seen gcs 11 on cpap come back to a lethargic 15, but I have never used it on such a pt.

I MIGHT give a brief trial while I got the RSI stuff out, but a GCS of 11 is fairly frank respiratory failure and it's time to knock the patient down.

 

[BLS Systems Limited]

Blindside makes some interesting points. The issue with administering positive pressure to a hypotensive patient is that the increased intrathoracic pressures created by positive pressures could exacerbate the hypotension (or so the theory states). Working in hospitals, respirologists and cardiologists are often at odds between lowering PEEP levels or giving vasopressors. The respirologist normally orders high PEEP to recruit the alveoli and giving vasopressors while the cardiologists order lowering the PEEP to minimize therapeutics (less is more kind of thing). At least that's my experience working in several hospitals.

 

[blindsideflank]

Your generally looking at CPAP decreasing workload as your shedding preload.

Will dropping preload in this patient cause a reflex and thus a harder working, less efficient heart (increase mvo2)... That doesn't really make sense but I hope you are getting what I mean.

It the body wants a pressure of 130 and you drop the pressure/preload the the body will work harder to try to get that 130.... Seems weird to think like this though because the body wouldn't compensate for nitro like this. Maybe if I don't think out loud I won't sound stupid

 

[usalsfyre]

Will dropping preload in this patient cause a reflex and thus a harder working, less efficient heart (increase mvo2)... That doesn't really make sense but I hope you are getting what I mean.

It the body wants a pressure of 130 and you drop the pressure/preload the the body will work harder to try to get that 130.... Seems weird to think like this though because the body wouldn't compensate for nitro like this. Maybe if I don't think out loud I won't sound stupid

I think I get what your saying, not a stupid question at all. Are you asking if dropping preload via CPAP will cause reflex tachycardia leading to a worsened MvO2?

Dropping preload is dropping preload, the mechanism isn't important (grossly oversimplified for the purposes of discussion). The kidneys attempting to keep the patient hypertensive is killing the LV in this case, your highly unlikely to make your MvO2 worse.